Does Resorting to Online Dispute Resolution Promote Agreements? Experimental Evidence

This paper presents the results of an experiment performed to test the properties of an innovative bargaining mechanism (called automated negotiation) used to resolve disputes arising from Internet-based transactions. Automated negotiation is an online sealed-bid process in which an automated algorithm evaluates bids from the parties and settles the case if the offers are within a prescribed range. The observed individual behavior, based on 40 rounds of bargaining, is shown to be drastically affected by the design of automated negotiation. The settlement rule encourages disputants to behave strategically by adopting aggressive bargaining positions, which implies that the mechanism is not able to promote agreements and generate efficiency. This conclusion is consistent with the experimental results on arbitration and the well-known chilling effect: Automated negotiation tends to "chill" bargaining as it creates incentives for individuals to misrepresent their true valuations and discourage them to converge on their own. However, this perverse effect induced by the settlement rule depends strongly on the conflict situation. When the threat that a disagreement occurs is more credible, the strategic effect is reduced since defendants are more interested in maximizing the efficiency of a settlement than their own expected profit.Online Dispute Resolution, Arbitration, Experimental Economics, Electronic Commerce, Bargaining

Does Resorting to Online Dispute Resolution Promote Agreements? Experimental Evidence

This paper presents an experiment performed to test the properties of an innovativebargaining mechanism (called automated negotiation) used to resolve disputes arising fromInternet-based transactions. The main result shows that the settlement rule tends to chillbargaining as it creates incentives for individuals to misrepresent their true valuations, whichimplies that automated negotiation is not able to promote agreements. However, this perverseeffect depends strongly on the conflict situation. When the threat that a disagreement occurs ismore credible, the strategic effect is reduced since defendants are more interested inmaximizing the efficiency of a settlement than their own expected profit. The implications ofthese results are then used to discuss the potential role of public regulation and reputationmechanisms in Cyberspace: Online Dispute Resolution, Electronic Commerce, Bargaining, Arbitration,Experimental Economics

Does Resorting to Online Dispute Resolution Promote Agreements ? Experimental Evidence

Working Paper du GATE 2004-01This paper presents the results of an experiment performed to test the properties of an innovative bargaining mechanism (called automated negotiation) used to resolve disputes arising from Internetbased transactions. Automated negotiation is an online sealed-bid process in which an automated algorithm evaluates bids from the parties and settles the case if the offers are within a prescribed range. The observed individual behavior, based on 40 rounds of bargaining, is shown to be drastically affected by the design of automated negotiation. The settlement rule encourages disputants to behave strategically by adopting aggressive bargaining positions, which implies that the mechanism is not able to promote agreements and generate efficiency. This conclusion is consistent with the experimental results on arbitration and the well-known chilling effect: Automated negotiation tends to “chill” bargaining as it creates incentives for individuals to misrepresent their true valuations and discourage them to converge on their own. However, this perverse effect induced by the settlement rule depends strongly on the conflict situation. When the threat that a disagreement occurs is more credible, the strategic effect is reduced since defendants are more interested in maximizing the efficiency of a settlement than their own expected profit.Ce papier présente les résultats d'une expérience dont l'objectif est de tester les propriétés d'un nouveau mécanisme de résolution des litiges électroniques (la négociation automatisée). Cette procédure consiste en un programme informatique accessible en ligne qui analyse les propositions d'accord émises par les parties et règle le différend si ces offres appartiennent à un intervalle prédéterminé. Le comportement individuel, observé sur 40 périodes de négociation, apparaît comme fortement influencé par le design de la procédure. La règle de négociation considérée incite les parties à adopter un comportement agressif, ce qui limite la capacité du mécanisme à favoriser la résolution du litige. Conformément aux résultats expérimentaux relatifs à la procédure d'arbitrage, la négociation automatisée crée un effet de glaciation tel que les individus ne sont pas incités à révéler leurs véritables valeurs de réserve et à trouver un accord par eux-mêmes. Cependant, cet effet pervers dépend fortement de l'intensité du conflit opposant les parties. Lorsque la menace d'un désaccord gagne en crédibilité, l'effet stratégique diminue dans la mesure où les défendeurs utilisent la procédure de manière plus efficiente afin de maximiser la probabilité de résolution du litige

Aging Independently of the Hormonal Status Changes Pain Responses in Young Postmenopausal Women

Both aging and hormonal status have an effect on pain perception. The goal of this study was to isolate as much as possible the effect of aging in postmenopausal women. Thirty-two women with regular menstrual cycles (RMW) and 18 postmenopausal women (PMW) underwent a 2-minute cold pressor test (CPT) to activate DNIC with a series of tonic heat pain stimulations with a contact thermode to assess ascending pain pathways. We found that this procedure induced much less pain during the first 15 seconds of stimulation the PMW group (P = 0.03), while the mean thermode pain ratings, pain tolerance, pain threshold, and DNIC analgesia were similar for both groups (P > 0.05). The absence of the peak pain in the PMW was probably due to reduced function of the myelinated Aδ fibers that naturally occurs with age

The effect of conditioning stimulus intensity on conditioned pain modulation (CPM) hypoalgesia

Contexte: L’ampleur et la durée de la modulation de la douleur conditionnée (MDC) dépendent probablement de la nature et de l’intensité du stimulus de conditionnement. Objectifs: Le but de cette étude était de mesurer l’effet de l’intensité du stimulus de conditionnement sur la durée de l’hypoalgésie par MDC. Méthodes: Dans cette étude en simple aveugle, non randomisée, à mesures répétées, nous avons évalué l’hypoalgésie par MDC chez 20 participants en bonne santé à la suite de tests au froid à 7 ° C et 12 ° C. Le stimulus du test, une stimulation thermique de 60 secondes, a été administré avant le test au froid et immédiatement après, puis à nouveau à des intervalles de cinq minutes jusqu’à ce que les scores de douleur des participants reviennent aux niveaux antérieurs au stimulus de conditionnement. Deux seuils d’hypoalgésie ont été utilisés pour établir le retour au niveau antérieur au stimulus de conditionnement : à l’intérieur de - 10 / 100 de la situation de départ et à l’intérieur de - 20 / 100 de la situation de départ. Résultats: L’hypoalgésie par MDC, définie comme une réduction des niveaux de douleur > 10 / 100, n’a pas duré plus longtemps après le test au froid plus intense de 7 ° C que le test au froid de 12 ° C (32 minutes comparativement à 20 minutes, respectivement ; P = 0,06) ; des résultats similaires ont été obtenus lorsque l’hypoalgésie par MDC était définie comme une réduction des niveaux de douleur > 20 / 100 (16 minutes après le test au froid à 7 ° C comparativement à 9 minutes après le test au froid à 12 ° C ; P = 0,33). La durée de l’hypoalgésie par MDC était significativement plus longue lorsque le seuil 10 / 100 était utilisé comparativement au seuil 20 / 100, quelle que soit la température du test au froid (P = 0,008 pour le test au froid à 12 ° C ; P < 0,001 pour le test au froid à 7 ° C). Conclusions: Le stimulus de conditionnement plus intense n’a pas induit d’hypoalgésie par MDC de plus longue durée comparativement au stimulus de conditionnement moins intense. Le choix du seuil pour ce qui constitue une hypoalgésie par MDC a eu un effet significatif sur les résultats.Abstract : Background: The magnitude and duration of conditioned pain modulation (CPM) likely depends on the nature and intensity of the conditioning stimulus (CS). Aims: The aim of this study was to measure the effect of CS intensity on the duration of CPM hypoalgesia. Methods: In this single-blind, nonrandomized, repeated measures study, we assessed CPM hypoalgesia in 20 healthy participants following cold pressor tests (CPT) at 7°C and 12°C. The test stimulus, a 60-s heat stimulation, was administered before the CPT and immediately after, and again at 5-min intervals until participants’ pain scores returned to pre-CS levels. Two hypoalgesia thresholds were used to establish return to pre-CS level: within −10/100 of baseline and within −20/100 of baseline. Results: CPM hypoalgesia, when defined as a reduction in pain levels >10/100, did not last longer following the more intense 7°C CPT compared to the 12°C CPT (32 min vs. 20 min, respectively; P = 0.06); similar results were obtained when CPM hypoalgesia was defined as a reduction in pain levels of >20/100 (16 min following the 7°C CPT vs. 9 min following the 12°C CPT; P = 0.33). The duration of CPM hypoalgesia was significantly longer when the 10/100 threshold was used compared to the 20/100 threshold, regardless of CPT temperature (P = 0.008 for the 12°C CPT; P < 0.001 for the 7°C CPT). Conclusions: The more intense CS did not induce CPM hypoalgesia of longer duration compared to the less intense CS. The choice of threshold for what constitutes CPM hypoalgesia did have a significant effect on the results

Serum Markers of Hepatocyte Death and Apoptosis Are Non Invasive Biomarkers of Severe Fibrosis in Patients with Alcoholic Liver Disease

BACKGROUND: Quantification of hepatocyte death is useful to evaluate the progression of alcoholic liver diseases. Our aims were to quantify and correlate the circulating levels of Cytokeratin 18 (CK18) and its caspases-generated fragment to disease severity in heavy alcoholics. METHODOLOGY/PRINCIPAL FINDINGS: CK18 and CK18-fragment were evaluated in the serum of 143 heavy alcoholics. Serum levels of markers of hepatocyte death (CK18), apoptosis (CK18 fragment) and necrosis (CK18 -CK18 fragment) increased in patients with severe fibrosis compared to patients with mild fibrosis. These markers strongly correlated with Mallory-Denk bodies, hepatocyte ballooning, fibrosis and with hepatic TNFα and TGFβ assessed in the liver of 24 patients. Elevated levels of serum hepatocyte death and apoptotic markers were independent risk factors in predicting severe fibrosis in a model combining alkaline phosphatase, bilirubin, prothrombin index, hyaluronate, hepatocyte death and apoptotic markers. The level of markers of hepatocyte death and apoptosis had an area under the receiving operator curve that predicted severe fibrosis of 0.84 and 0.76, respectively. CONCLUSION/SIGNIFICANCE: Death of hepatocytes can be easily evaluated with serum markers and correlated with severe fibrosis in heavy alcohol drinkers. These biomarkers could be useful to rapidly evaluate liver injuries and the efficacy of therapies

Cannabinoid CB2 Receptor Potentiates Obesity-Associated Inflammation, Insulin Resistance and Hepatic Steatosis

BACKGROUND: Obesity-associated inflammation is of critical importance in the development of insulin resistance and non-alcoholic fatty liver disease. Since the cannabinoid receptor CB2 regulates innate immunity, the aim of the present study was to investigate its role in obesity-induced inflammation, insulin resistance and fatty liver. METHODOLOGY: Murine obesity models included genetically leptin-deficient ob/ob mice and wild type (WT) mice fed a high fat diet (HFD), that were compared to their lean counterparts. Animals were treated with pharmacological modulators of CB2 receptors. Experiments were also performed in mice knock-out for CB2 receptors (Cnr2 -/-). PRINCIPAL FINDINGS: In both HFD-fed WT mice and ob/ob mice, Cnr2 expression underwent a marked induction in the stromal vascular fraction of epididymal adipose tissue that correlated with increased fat inflammation. Treatment with the CB2 agonist JWH-133 potentiated adipose tissue inflammation in HFD-fed WT mice. Moreover, cultured fat pads isolated from ob/ob mice displayed increased Tnf and Ccl2 expression upon exposure to JWH-133. In keeping, genetic or pharmacological inactivation of CB2 receptors decreased adipose tissue macrophage infiltration associated with obesity, and reduced inductions of Tnf and Ccl2 expressions. In the liver of obese mice, Cnr2 mRNA was only weakly induced, and CB2 receptors moderately contributed to liver inflammation. HFD-induced insulin resistance increased in response to JWH-133 and reduced in Cnr2 -/- mice. Finally, HFD-induced hepatic steatosis was enhanced in WT mice treated with JWH-133 and blunted in Cnr2 -/- mice. CONCLUSION/SIGNIFICANCE: These data unravel a previously unrecognized contribution of CB2 receptors to obesity-associated inflammation, insulin resistance and non-alcoholic fatty liver disease, and suggest that CB2 receptor antagonists may open a new therapeutic approach for the management of obesity-associated metabolic disorder

Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy

Mammalian target of rapamycin (mTOR) is a key regulator of cell growth that associates with raptor and rictor to form the mTOR complex 1 (mTORC1) and mTORC2, respectively. Raptor is required for oxidative muscle integrity, whereas rictor is dispensable. In this study, we show that muscle-specific inactivation of mTOR leads to severe myopathy, resulting in premature death. mTOR-deficient muscles display metabolic changes similar to those observed in muscles lacking raptor, including impaired oxidative metabolism, altered mitochondrial regulation, and glycogen accumulation associated with protein kinase B/Akt hyperactivation. In addition, mTOR-deficient muscles exhibit increased basal glucose uptake, whereas whole body glucose homeostasis is essentially maintained. Importantly, loss of mTOR exacerbates the myopathic features in both slow oxidative and fast glycolytic muscles. Moreover, mTOR but not raptor and rictor deficiency leads to reduced muscle dystrophin content. We provide evidence that mTOR controls dystrophin transcription in a cell-autonomous, rapamycin-resistant, and kinase-independent manner. Collectively, our results demonstrate that mTOR acts mainly via mTORC1, whereas regulation of dystrophin is raptor and rictor independent